It is the long range goal of this project to determine whether tumor promotion by various agents, e.g., phorbol esters, proceeds via the release of arachidonic acid (AA) and the subsequent synthesis of prostaglandins (PG) by hydroxy fatty acid (HFA). We have examined several fibroblasts and chosen the mouse embryo fibroblast (10T 1/2) as a model system. PG production by these cells was examined with respect to cell growth and cell density. Phorbol esters (TPA) altered cell growth and PG plus HFA production. Our goal is to differentiate between the release of AA, formation of PGs and HFAs by use of selective inhibitors of these pathways.